L16 - Sleep and Behavioural Disorders Flashcards

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1
Q

What is insomnia?

A

Difficulty initiating/maintaining sleep.

  • Sleep onset over 20-30 minutes.
  • waking up after sleep onset
  • 3 times per week for more than 4 weeks

NEED TO HAVE DAYTIME DISTRESS/IMPAIRMENT

Most common sleep disorder, found in 10% of aus pop

Bi directional relationship w/ mental health.
- Is a risk factor for future mood disorders, and can be caused by psychiatric disorders as a comobidity

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2
Q

Hyperarousal in Insomnia?

A

ELEVATED CORTICAL AROUSAL

  • increased cognitive activity, sensory & info processing
  • EEG: Higher frequency power during REM & NREM (not delta waves, which are slow freq). Shows that they’re in lighter sleep stages, and thus are more easily woken
  • More likely to elicit an evoked response in brain waves after playing auditory stimuli, during wake and sleep onset.
  • not sleepy, 24-hr hyper arousal.

ELEVATED PHYSIOLOGICAL AROUSAL

  • autonomic NS - increased HR (pre-sleep and sleep), Symp NS, decrease Parasymp NS (sleep)
  • increase whole-body metabolic rate
  • increase core body temp, day and night
  • increased night time cortisol
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3
Q

Treatment for insomnia?

A
  • CBTI, longer lasting benefit than sedatives

sleep hygiene and education, sleep restriction based on sleep diary reports, stimulus control, cognitive restruturing (you can work if you don’t sleep well, dont worry) to reduce associated anxiety.

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4
Q

link b/w depression and insomnia?

A

50% of patients w/ depression have comorbid insomnia.

  • Reduced total sleep time, sleep efficiency, SWS%, REM latency, and increased sleep onset latency and REM%
  • more awakenings during the night, early REM and decreased REM amount
  • treating with CBTI helped BOTH the insomnia and the depression! almost doubles remission rate.
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5
Q

Link b/w sleep and depression?

A
  • chronic sleep dep increases risk for depression
  • acute sleep dep has antidepressant effects, due to high adenosine acting on A1 receptors, and increased cortisol.
  • same effect if you just wake up in the morning and miss most of REM sleep..
  • SSRIs usually abolish or greatly reduce REM.

Might be helpful becuase the rem-off neurons include the RAPHE NUCLEUS which releases serotonin!

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6
Q

Sleep in bipolar disorder?

A
  • sleep disturbance is a key symp –> reduced NEED FOR SLEEP during manic, and insomnia/hypersomnia in depressive phase.
  • sleep dist is the most common prodrome for mania, and 6th most common prodrome for depression.
  • sleep dep can drigger episode
  • actigraphy shows cyclic pattern, correlation between manic phase - no sleep and deprssive phase - sleep.
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7
Q

Sleep and schizophrenia?

A
  • 45% of patients have comorbid insomnia
  • Reduced total sleep time, sleep efficiency and increased Sleep onset latency.
  • reduced sleep spindles. normal REM and SWS
  • sleep disturbances appear to predisphose scz
  • CBTI improved delusion
  • circadian phase abnormalities - can sleep at all stages of 24hr period, delayed/freerun
  • delayed sleep phase persists with treatment in 50% people
  • sleep disturbances remain post treatment even once circadian rhythm is restord.
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8
Q

Delayed sleep phase in scz?

A
  • circadian phase abnormalities - can sleep at all stages of 24hr period, delayed/free run
  • delayed sleep phase persists with treatment in 50% people
  • sleep disturbances remain post treatment even once circadian rhythm is restored.

possible reasons:

  • lack of imposed schedules, eg. work
  • lack of light exposure
  • drug effects, excess dopaminergic activity
  • no evidence of Ach, orexin or gaba involvement
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9
Q

ADHD and sleep?

A
  • Symptoms overlap with symptoms of children who lack sleep –> hyperactivity
  • treatment of sleep disorder can abolish adhd symptoms
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10
Q

Sleep and depression in adolescence?

A
  • vulnerable time for depression, also associated with many other changes - hormonal, sleep, circadian rhythm, lifestyle factors.
  • EEG shows decrease in delta and theta power asa function of age –> reduce in SWS.
  • due to synaptic pruning, simplying the connections made in childhood.
  • can see that synaptic density decreases across adolescence to reach a level in adulthood that is similar to that of birth.
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11
Q

Circadian changes across early adolescence?

A
  • homeostatic drive produces over adolescence - need for sleep dramatically changes over that time (homeostatic drive reduces)
  • When compared to prepubernal kids, post pubernal group had greater sleep latency periods from 10:30-2:30 in the morning.
  • melatonin release was offset by about 1 hour.

CIRCADIAN PHASE DELAY

  • seen in all cultures
  • seen in animals at dev equiv points
  • can also be impacted by other societal changes
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12
Q

What are some social-cultural factors that could impact the circadian phase delay in adolescents?

A
  • factors encouraging adolescents to remain awake in the evening, eg. homework.
  • household lighting can impact phase shifting, causing delayed wakefullness.
  • time of awakening - constrained by school, causing sleep deprivation. can be seen in rebound recovery sleep during weekend and school holidays
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13
Q

What did the ‘SENSE’ study find?

A

Sleep intervention on at-risk adolescents

Experimental group - CBT and mindfulness based sleep intervention
Control - study education

findings:

  • sleep group improved in subjective (daytime sleepiness) and objective measures of sleep, particularly sleep onset latency, by sticking to stricter schedule
  • decreased anxiety related symptoms - sep anx and obsessive compulsive
  • sig benefit to sleep group tended to related to pre-intervention problem areas (SOL and anxiety)
  • effects on depression not measured
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